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Cardiovascular System (Drugs Affecting Coagulation)


The cardiovascular system serves essential functions in the body. Among its position is the coagulation process, which begins physiologically when blood vessels are injured. This coagulation process is facilitated by platelets and other factors in the body (Breitenstein et al., 2010). when this physiologic process is disrupted, it results in the development of coagulopathies that need to be managed with drugs to maintain the cardiovascular system’s physiologic function. These coagulopathies may either be abnormal blood clotting or excessive bleeding due to the inability of the blood to clot properly. Drugs are prescribed to manage these coagulopathies; for instance, if the blood clots unnecessarily, the person is specified blood thinners, among others, to prevent abnormal clot formation, while if the blood does not clot when it should, the person is prescribed coagulants to facilitate clotting. In this paper, the various drugs that affect coagulation will be discussed.

Drugs Affecting Coagulation

  • Aspirin

Aspirin causes a lasting operational impairment in platelets, which may be seen in clinical practice as a longer hemorrhage time. This seems to be related to permanent inhibition of a crucial enzyme in platelet arachidonate conversion owing to acetylation of a vital serine molecule within its catalytic site. Aspirin is the drug of choice to treat or prevent blood clots in cardiovascular diseases, like coronary artery disease. Primarily;

  1. a significant decrease in platelet suppression is linked with less than maximum COX-1 inhibition;
  2. platelet functionality restitution is abnormally quick, happening within 3–4 days after medication withdrawal,
  3. Most standard non-steroidal anti-inflammatory medications (NSAIDs) cannot provide almost complete and long-lasting inhibition of platelet COX-1, enabling their COX-2-dependent cardiotoxicity to be revealed.
  4. Furthermore, Aspirin’s suppression of TXA2-dependent platelet function leaves other platelet pathways substantially unchanged, arguing for dual or triple antiplatelet treatment in high-risk scenarios.

However, there are various adverse effects of Aspirin, most notably excessive bleeding. Sine is used to preventing blood clots. The drug can also cause hemorrhages, with gastrointestinal blooding, particularly the most common in the small intestine and stomach, and brain hemorrhage the most fatal. A combination of Aspirin and other medications, especially anticoagulants, should be done carefully to minimize the risk of bleeding (Johnson et al., 2008).

  • Warfin

Warfin is another oral anticoagulant, taken once a day and used widely. It has been used extensively for the treatment of thromboembolic disorders for years. Such thromboembolic diseases include deep vein thrombosis and stroke in patients with atrial fibrillations. It functions to prevent the regeneration of vitamin K, which is an essential component of the blood clotting process. Therefore, when vitamin K production is inhibited, the blood clotting process cannot continue, and consequently, no clots are formed. Dosing of Warfin has been a challenge because different people respond differently to the drug. This has been attributed to the genetic makeup of other individuals, and researchers argue that genotyping would be essential to ensure that patients on Warfin receive the proper drug doses.

Like Aspirin, Warfin has been associated with bleeding and easy bruising. It is contraindicated in individuals with hypertension, and individuals taking it should perform a blood test at least once in three months to ensure that they are taking the correct dose (Hanley, 2004).

  • Reteplase and Alteplase

Reteplase (rPA) is a 355 amino acid excision of tPA containing just the K2 and S modules of Alteplase, with a molecular mass of thirty-nine kilodaltons (Mohammadi et al., 2019). rPA has higher thrombolytic efficacy than Alteplase (Hanover et al., 2005). When the F, EGF, and K1 subdomains of rPA are deleted, the plasma half-life is prolonged, the fibrin specificity is decreased, and the capacity to enter blood clots is improved (Mohammadi et al., 2019). Due to eliminating the fibronectin fingers section, rPA’s ability to bind fibrin is decreased. Conversely, higher affinities for fibrin have been demonstrated using chimeric and mutant rPA (Raigani et al., 2017).

Reteplase (rPA) is a variation of Alteplase (tPA) that retains two functional portions of the protease, namely the thrombolytic Kringle2 and the protease domain, and the N-terminal 1–3 amino acid segments. Compared to indigenous tPA, rPA has a prolonged plasma half-life, improved clot diffusion, and increased fibrinolytic activity (Mohammadi et al., 2019). The clinical research investigation established that reteplase is a successful and safe treatment for PTE (pulmonary thromboembolism). A bit of dose of reteplase exhibits effectiveness equivalent to that of Alteplase. The study revealed that Reteplase and Altplase might have therapeutic use as a therapy for PTE as Thrombolytic Agents.

  • Cilostazol

Cilostazol, a powerful phosphodiesterase class III selectivity inhibitor, is the only vasodilation and antiproliferative medication with established evidence (grade IA) in the therapy for PAD whenever used with conventional antiplatelet medicines (Gerhard-Herman et al., 2017). Cilostazol has indeed been proven to enhance walking distances in patients with periodic claudication (Fontaine’s stage IIA or IIB) (Bedenis et al., 2014) and therefore is currently approved as the first-line treatment for low extremities PAD up to and including advanced phase IIB.

Additionally, it significantly lowered restenosis following surgical and endovascular treatments in patients with severe ischemia, demonstrating intermediate long-term effectiveness and an attenuated incidence of hemorrhagic sequelae (Soga et al., 2011). Cilostazol dramatically decreased the incidence of restenosis and increased the rate of principal patency in patients receiving femoropopliteal stenting, particularly in individuals at significant threat of stents restenosis. Additionally, it is the only drug that has shown good effectiveness in reducing the incidence of restenosis following coronary or periphery revascularization operations in randomized managed studies (de Donato et al., 2017). It is well established that increasing the amount of antiaggregant and anticoagulation medications raises the likelihood of hemorrhage episodes in older people.

  • Oral Anticoagulants (Rivaroxaban, Dabigatran and Apixaban)

Unlike conventional oral vitamin K antagonists (VKAs), innovative oral anticoagulants (OACs) are administered at predetermined dosages and have a lesser possibility for medication and dietary issues (Ageno et al., 2012). Like VKAs like warfarin, these medicines have comparable effectiveness, and safety attributes to known parenteral medications like unfractionated heparin (Ageno et al., 2012). New OACs include rivaroxaban, dabigatran, and apixaban.

These and other medicines are being studied to treat numerous thromboembolic diseases. Adults undergoing elective hip or knees replacements surgery are currently able to take rivaroxaban, a straight Factor Xa inhibitor, for two weeks or five weeks to avoid venous thromboembolism (Janssen Pharmaceuticals Inc, 2013). Both apixaban and dabigatran are currently licensed in the EU for orthopedic use. Also, rivaroxaban is approved for the therapy of deep venous thrombosis (DVT) and pulmonary embolism (PE) in individuals (Janssen Pharmaceuticals Inc, 2013). In individuals with non-valvular AF, apixaban, and dabigatran are approved to lower the risks of strokes and systemic embolism (Lip et al., 2016).

Rivaroxaban with acetylsalicylic acid (ASA) solo or ASA combined clopidogrel or ticlopidine is appropriate for protecting atherothrombotic occurrences in elderly patients with increased cardiac biomarkers following ACS. The new OACs work by directly addressing specific coagulation cascades components. The comprehensive characterization of these medicines’ PK and PD characteristics was crucial for their clinical advancement.

A thorough collection of phases I and II research addressing PK and PD in healthy persons and patients taking the medication for active protection or therapy of thrombosis (Mueck et al., 2011) backed this rivaroxaban phase III clinical trial program. These investigations also characterized other essential characteristics of rivaroxaban, including few clinically meaningful drug-drug associations. Rivaroxaban and other innovative OACs do not need frequent coagulation management (Ageno et al., 2012).


To ensure efficient implementation, practitioners must intervene by examining patients for symptoms of blood loss to establish the efficacy of treatment and to encourage rapid action during bleeding occurrences. Second, they should institute safety steps to safeguard the patient’s wellbeing. Third, they should assess efficacy by monitoring coagulation investigations and making necessary dosage adjustments. Notably, physicians should educate patients on drug treatment, such as the medicine’s names, rationale, and potential adverse effects, to increase patient comprehension and boost compliance to the dosing prescription.


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Bedenis, R., Stewart, M., Cleanthis, M., Robless, P., Mikhailidis, D. P., & Stansby, G. (2014). Cilostazol for intermittent claudication. Cochrane Database of Systematic Reviews, (10).

Breitenstein, A., Camici, G. G., & Tanner, F. C. (2010). Tissue factor: beyond coagulation in the cardiovascular system. Clinical Science118(3), 159-172.

de Donato, G., Setacci, F., Mele, M., Giannace, G., Galzerano, G., & Setacci, C. (2017). Restenosis after coronary and peripheral intervention: efficacy and clinical impact of cilostazol. Annals of vascular surgery41, 300-307.

Gerhard-Herman, M. D., Gornik, H. L., Barrett, C., Barshes, N. R., Corriere, M. A., Drachman, D. E., … & Walsh, M. E. (2017). 2016 AHA/ACC guideline on managing patients with lower extremity peripheral artery disease: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Journal of the American College of Cardiology69(11), e71-e126.

Hanover, T. M., Kalbaugh, C. A., Gray, B. H., Langan, E. M., Taylor, S. M., Androes, M. P., … & Blackhurst, D. W. (2005). Safety and efficacy of reteplase for treating acute arterial occlusion: the complexity of underlying lesion predicts outcome. Annals of vascular surgery19(6), 817-822.

Hanley, J. P. (2004). Warfarin reversal. Journal of Clinical Pathology57(11), 1132-1139.

Janssen Pharmaceuticals Inc: (2013) XareltoW (rivaroxaban) prescribing information.

Johnson, S. G., Rogers, K., Delate, T., & Witt, D. M. (2008). Outcomes associated with combined antiplatelet and anticoagulant therapy. Chest133(4), 948-954.

Lip, G. Y., Keshishian, A., Kamble, S., Pan, X., Mardekian, J., Horblyuk, R., & Hamilton, M. (2016). Real-world comparison of significant bleeding risk among non-valvular atrial fibrillation patients initiated on apixaban, dabigatran, rivaroxaban, or warfarin. Thrombosis and haemostasis116(11), 975-986.

Mohammadi, E., Seyedhosseini-Ghaheh, H., Mahnam, K., Jahanian-Najafabadi, A., & Sadeghi, H. M. M. (2019). Reteplase: structure, function, and production. Advanced biomedical research8.

Mueck, W., Lensing, A. W., Agnelli, G., Decousus, H., Prandoni, P., & Misselwitz, F. (2011). Rivaroxaban. Clinical pharmacokinetics50(10), 675-686.

Raigani, M., Rouini, M. R., Golabchifar, A. A., Mirabzadeh, E., Vaziri, B., Barkhordari, F., & Mahboudi, F. (2017). Scale-up and pharmacokinetic study of a novel mutated chimeric tissue plasminogen activator (mt-PA) in rats. Scientific reports7(1), 1-12.

Soga, Y., Iida, O., Hirano, K., Suzuki, K., Kawasaki, D., Miyashita, Y., … & Nobuyoshi, M. (2011). Impact of cilostazol after endovascular treatment for infrainguinal disease in patients with critical limb ischemia. Journal of vascular surgery54(6), 1659-1667.


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